February 23, 2009
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Insulin may be effective treatment for Alzheimer’s disease

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By shielding memory-forming synapses from harm, insulin may slow or prevent damage and memory loss caused by toxic proteins in Alzheimer’s disease, according to the findings from a recent trial.

The researchers investigated synapse pathology in mature cultures of hippocampal neurons. They treated the cells with insulin and rosiglitazone and found that damage to neurons exposed to amyloid beta-derived diffusible ligands was blocked by insulin, keeping amyloid beta-derived diffusible ligands from attaching to the cells. Protection by low levels of insulin was enhanced by rosiglitazone as well, according to a press release.

Insulin failed to block amyloid beta-derived diffusible ligand binding when insulin receptor tyrosine kinase activity was inhibited, according to the researchers. There was an increase in binding caused by insulin receptor inhibition.

According to the researchers, the protective role of insulin derives from insulin receptor signaling-dependent downregulation of amyloid beta-derived diffusible ligand binding sites rather than from ligand competition.

“Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer’s disease,” the researchers wrote in a press release.

“Sensitivity to insulin can decline with aging, which presents a novel risk factor for Alzheimer’s disease; our results demonstrate that bolstering insulin signaling can protect neurons from harm,” they wrote.

Proc Natl Acad Sci U S A. 2009;106:1971-1976.